Rheumatology Flashcards
RA: define
chronic systemic inflammatory disease
synovial joints
symmetrical deforming polyarthritis
RA: pathophysiology
not fully understood
genetically susceptible individuals + unknown antigen
-> autoimmune response
-> synovitis of joints and tendon sheaths
-> synovial hypertrophy
-> cartilage damage
-> bone destruction
T cells stimulate inflammatory cytokines
-> TNF-alpha, IL-1, IL-6 -> pro-inflammatory state
RA: risk factors
pre-menopausal women family history smoking infection diet hormonal
RA: age of onset
20-40 years
RA: clinical features
Stiffness (morning >1 hour) Symmetrical Swollen joints (polyarthritis) Small joints of the hand and feet Sex (female:male 3:1) Speed: quick onet over weeks of months Specific signs in the hand: - early: swollen MCP, PIP and MTS joints - late: Boutonnieres deformity, swan neck deformity, ulnar deviation, z-deformity of the thumb
RA: hand features
- early: swollen MCP, PIP and MTS joints
- late: Boutonnieres deformity, swan neck deformity, ulnar deviation, z-deformity of the thumb
Boutonniere deformity define
flexion of the PIP
hyperextension of DIP
Swan neck deformity
hyperextension of PIP
flexion of DIP
RA: extra-articular manifestations
dry eyes, scleritis pulmonary fibrosis lymphadenopathy anaemia rheumatoid nodules Stomach ulcers & renal disease (drug related) vasculitis osteoporosis
RA and OA comparison
RA symmetrical, OA not RA morning stiffness >1h, OA <30min RA not worse on movement, OA is RA onset at 20-40 year old, OA >50 RA rapid onset, OA takes years RA has systemic symptoms, OA doesn't RA worse in the morning, OA evening
RA: diagnosis
history 6 weeks + 3+ swollen tender joints, symmetrical positive investigations ( rheumatoid factor, anti-CCP, ESR, CPR
RA: investigations
rheumatoid factor (high sensititvity, low specificity)
anti-CCP (low sensitivity, high specificity)
ESR
CRP
RA: management
start within 3 m. of symptom onset
DMARDs (disease modifying anti-rheumatic drugs) combination of 2
- methotrexate
-sulfasalazine
- hyroxychloroquine
Corticosteroids injection/oral for rapid relief
NSAIDS for symptomatic relief and red. inflammation
TNF- alpha inhibitos (infliximab)
B-cell blockers (rituximab)
physiotherapy
rheumatology referral
surgery for pain relief and deformity/function restoration
Disease Activity score (DAS) 28: what joints are included
MCP, PIP, wrist Elbows Shoulders Knees 28 joints
Disease Activity Score (DAS) 28: what disease is it used in?
RA
Disease Activity score (DAS) 28: what is taken into accont
tenderness and swelling at 28 joints
ESR
self-reported symptom severity
RA: monitoring
CRP
DAS28 (Disease activity score)
RA: radiological features
LESS Loss of joint space Erosions Soft tissue swelling Soft bones- oseopenia
OA: define
condition characterised by cartilage damage joint space narrowing -> pain, functional limitation and impaired quality of life any joint
OA: pathophysiology
metabolically dynamic process
imbalance between breakdown and bone repair
normally, hyaline (articulating) cartilage: collagen and matrix components get degraded and replaced by chondrocyte cells
OA: apoptosis of chondrocytes
-> cytokines (IL-1, TNF- alfa)
-> protease enzymes (metalloproteases)
- > cartilage destruction (thinning and fibrillation)
- > abnormal subchondral bone growth
- > oseophytes and bone custs
OA: clinical features
joint pain
- worse on movement
- morning stiffness <30mins
- periarticular tenderness
- crepitus
- muscle wasting
- deformity
- instabilityy
- bouchard’s nodes
- heberden’s nodes
Difference between bouchard’s and heberden’s nodes ?
OA- hard/bony swellings
Bouchard’s nodes: PIP joints
Heberden’s nodes: DIP joints
OA: investigations
Bloods: ESR, CRP, RF, anti-CCP: all normal or negative
X ray: LOSS
MRI shows early changes
OA: X-ray features
LOSS Loss of joint space Osteophytes Subchondral sclerosis Subchondral cysts
OA: presentation questions
predisposing factors (trauma?)
PMH (secondary causes: RA, Paget’s disease)
Family hisotry
Occupation
OA: non-pharmacological management
education
exercise
weight loss
transcutaneous nerve stmulation (TENS)
Aids and devices: footwear, insoles, bracing
physiotherapy
Surgery: replacement, arthroscopic debridement
OA: pharmacological management
Paracetamol +/- topical NSAIDs
add wezak opioid (codeine)
add oral NSAID + PPI (red. inflammation)
intra-articular CS injections
Septic arthritis: define
acute infection (usually bacterial) of a native or prosthetic joint -> rapid joint destruction knee and hip most commonly affected
Septic arthritis: cause
haematogenous spread (respiratory or UTI)
local tissue infection (cellulitis and osteomyelitis)
penetrating trauma
inoculation
Septic arthritis: pathophysiology
bacteria in the joint
- > cytokines release
- > proteoglycans and collagen hydrolysis
- > cartilage destruction
- > bone loss
Septic arthritis: causative bacteria
gram +ve cocci:
-streptococcus aureus
-staphylococcus epidermis (in prosthetic joints)
gram-ve cocci:
- neisseria gonorrhae
gram -ve bacilli
- rara, mainly in diabetics, eldery and IV drug users
Septic arthritis: risk factors
prosthetic joint RA DM IV drug use Osteomyelitis Intra-articular injection/aspiration
Septic arthritis: clinical features
Red flags: -extremely painful -erythema -acutely swollen joint Muscle spasm/joint immobility systemic features: tachy, fevel, rash, malaise, anorexia loosening of the implant
Septic arthritis: investigations
joint aspiration +/- USS -> gram staining, WCC, culture, polarised light microscopy (ex: gout, CPPD) blood culture blood tests (sepsis) X-ray (normal/undelying joint disease)
Septic arthritis: management
Empiric/S.aureus: flucloxacillin IV -> PO/ Vancomycin Strep. pneumoniae: Benzylpenicilin IV -> Amoxivilin PO / Vancomycin IV -> Doxycycline PO Gram negative: ceftaxime IV
up to 14 days
Athocentesis, lavage, debridement
immobilisation -> physiotherapy
Monitoring w/ WCC, CRP, LFT’s, U&E’s
Spondyloarthopathies: conditions
PEAR Psoriatic arthritis Enteropathis spondyloarthropathies Ankylosing spondylitis Reactive arthritis
Spondyloarthropathies overlapping features
rheumatoid factor negative- seronegative
HLA-B27 association
axial arthritis
Asymmetrical large joints
Mono- or oligo-arthritis (<5 joints)
Enthesitis (inflam. of tendon or ligment insertion)
Dactylitis (sausage digit)
Extra articular manifestations like IBD or iritis
Psoriatic arthritis: define
chronic inflammatory arthritis
seronegative spondyloarthropathy
small joints of the hand
variable disease patterns
PsA: pathophysiology
poorly understood genetically susceptible indiv. exposed to an environmental trigger -> T-cell infiltration -> chemokine/cytokine release ->angiogenesis and cellular infiltration
PsA: risk factors
Psoriasis, usually before (70%), at the same time (5%) or after (25%)
family history (HLA-B27)
trauma
HIV
PsA: clinical features patterns
DR SAM
DIP joint disease Rheumatoid pattern (seronegative and lack of nodules) Spondyloarthritis (may be w/ usilated sacriliitis, typical or atypical AS) Asymmetrical oligoarthritis of large joints Mutilans arthritis (rare, severe form, osteolysis -> small joint destruction-> digits shorthening)
PsA: general clinical features
joint pain morning stiffness >30 mins Dactylitis (sausage digits) Enthesitis- pain at tendon/ligaments insertions into the bone Psoriatic rash naul changes (pitting, hyperkeratotis)
PsA: diagnosis
CASPAR criteria
Current psoriasis- 2pts History of psoriasis- 1pt Fam history of psoriasis- 1pt Dactylitis- 1pt Juxta-articular new bone formation -1pt RF neg -1pt Nail changes- 1pt
PsA: investigations
X-rays: soft tissue swelling, DIP joint erosion, periarticular new bone formation, oseolysis, pencil in cup deformity (advanced)
Bloods: ESR and CRP (normal or raised in active disease), RF, anti-CCP and ANA negative
PsA: management
NSAIDs DMARDs (Trial of 3m): Methotrexate + ciclosporin/ sufasalazine Intra articular CS injecitons Anti-TNF alpha theraphy (infliximab) Physiotherapy
Ankylosing spondylitis: define
chronic inflammatory disorder of the sacroiliac joints and spine
commonest seronegative spondyloarthropathy
other features: peripheral arthritis, enthesitis and extra-articular organ involvement
ankylosis = joint fusion
Ankylosing Spondylitis: pathophysiology
Genetic and environmental factors
HLA-B27 association
inflammation of sacroiliac joints
- IV disc, multiple joints and ligmaments involved
early: subchondral granulation tissue -> erosion -> fibrocartilage -> ossification at ligamentous and capsular attachement sites (enthesitis)
late: annulus fibrosis calcification -> bony bridge formation between verderbae (syndesmophytes)-> fusion
Syndesmophytes
bony bridge between vertebrae
seen in Anklylosing Spondylitis (annulus fibrosis calcification)
Ankylosing Spondylitis clinical features
dull back pain
stiffness >6 m
- both worse at night and early morning
- worse with rest
- better with exervise
reduced motion in lumbar spine (Schober’s test) and cervical spine
Question mark ? posture: loss of lumbar lordosis, thoracic kyphosis and neck hyperextension
Ankylosing Spondylitis extra-articular features
A- factor
Atlanto-axial subluxation Anterior uveitis Apical lung fibrosis Aortic incompetence AV node block Achilles tendinitis Amyloidosis (rare, late complication)
Question mark posture where is it seen?
Ankulosing sponylitis
Schober’s test, what is it and what does it signify?
Assessment of flexion of the spine
mark at the posterior superior illiac spines and 10cm above
forward spinal flexion to 13.5-15cm (normal)
reduced lumbar spine movement in ankylosing spondylitis
Ankylosing Spondylitis: investigations
X-ray: sacroiliitis grade- diagnostic
MRI- early changes
Bloods: CRP, ESR (both in active disease), RF and ANA negative, HLA-B27 testing
USS- enthesitis
Ankylosing Spondylitis: X-ray features
Sacroillitis grade - joint irregularity, scerosis, - joint space narrowing - joint fusion (anklylosis) Early changes - bone erosions - SI joint widening - square vertebral bodies with shiny corners Late changes - longitudinal lig. ossification - bamboo spine appearance
Bamboo spine appearance: where is it seen
Ankylosing Spondylitis
Ankylosing Spondylitis: management
exercise and physio NSAIDs -> codeine + paracetamol if insufficient local CS anti- TNF- alpha Surgery: replacements
Reactive arthritis: define
acute aseptic arthritis response to extra-articular infection (GI/GU tract) seronegative spondyloarthropathy asymetrical oligoarthritis usually in the lower limbs
Reactive arthritis: pathophysiology
infectious trigger (usually from bacterial GI/GU infection)
in genetically susceptible individuals
->immune activation with self-antigents
-> acute inflammation
usually 2-6 weeks after the initial infection
inflammation of joints, entheses, axial skeleton, mucous membranes, GI tract and eyes
HLA-B27 association
Reactive arthritis risk factors
GI/GU infection
Males (in relation to Chlamydia)
HLA-B27 positive
Caucasian patients
Reactive arthritis: clinical features
arthritis- acute, asymmetrical, large j. 2-6 wks after initial infection may be accompanied by malaise, fatigue and fever enthesitis conjunctivitis anterior uveitis dactylitis lower back pain mounth ulcers nail changes keratoderma blennorrgagica
Reactive arthritis: what skin condition is it associated with?
keratoderma blennorrhagica
Reactive arthritis: what syndrome is it associated with?
Reiter’s syndrome:
reactive arthritis
conjuctivitis
urethritis
Reiter’s syndrome: define
Reactive arthritis
conjuctivitis
urethritis
Reactive arthritis: investigations
Bloods
- raised: CRP, EST, leucocytosis and thrombocytosis (acute phase)
- ANA, RF, anti-CCP negative
- HLA-B27 positive in most
X-ray: usually normal +/- erosions, spurs, sacroiliitis
Joint aspirate (r.o cyrstal or septic arthritis) -> sterile, cloudy w/ raised WCC
stool, throat or urine culture- identify causative organism
serology for chlamydia
MRI if chronic
Reactive arthritis: management
rest + splint +/- physio
NSAIDS
intra- articular CS
DMARDs: methotrexate, sulfasalizine (for persisten or refractory disease)
Abs: tetracyclines for urethritis by Chlamydia
Anti-TNF alpha (in aggressive cases)
Gout; define
inflammatory arthritis
progresses from asymptomatic hyperuricaemia
urate crystals deposition in the synovial fluid
Gout: pathophysiology stages
asymptomatic hyperuricaemia (up to 20 years)
acute gout phase (serum lvls reach saturation -> deposition-> inflammatory response)
inter-critical gout phase (asymptomatic period between attacks)
chronic gout phase (chronic symptoms)
What is urate crystal?
a purine product
Hyperuraemia causes
impaired renal excretion
overproduction of uric acid
over-consumption of purine rich foods (metobalised to urate)
Gout: risk factors
hyperuricaemia
males
red meat, shellfish
alcohol -> ketones (compete with urate for renal excretion) also inc. risk via dehydration
Diuretics, aspirin, ciclosporin, laxatives
Chronic renal failure
Other: obesity, HTN, fam history, age, coronary heart disease, DM
Gout: clinical features
red flag: single peripheral joint, excruciating pain (oftern nocturnal- bed covers cause pain), red, hot and swollen
1st MTP joint (podargia), small joints of foot (mid-tarsal) and hand, the ankle, knee and elbow
chronic gout: polyarthritis, thopi (nodular subcutaneous urate deposits), fever and malaise
Gout of 1st MTP joint: name
podargia
Gout: hallmark of chronic gout
thophi
- nodular subcutaneous deposition of uric acid crystals
Gout: investigations
joint aspiration + synovial fluid analysis
-> negatively bifringent crystals under polarized light microscopy
- exclude septic arthritis
serum urate
X-ray: soft tissue swelling, late: punched out erosions
Gout: diagnois
Joint aspiration + synovial fuild analysis
-> negatively bifringent crystals under polarised light microscopy
Gout: management of acute gout
NSAIDs naproxen (+PPI)
Colchicine if NSAIDs contraindicated/not tolerated
Intra-articular CS (NSAIDs, Colchicine c/indicated, eg renal impairment)
Paracentamol +/- codeine- pain relief
Gout: management, prevention of acute atacks
Lifestyle changes (weight loss, reduce purines in diet, alcohol, regular exercise and stop smoking)
Allopurinol 1-2 weeks after acute phase
Febuxostat if allopurinol c/indicated
Pseudogout/CPPD: define
inflammatory arthritis
calcium purophosphate cristals deposition in the joint space
coexist with OA
most common cause of chondrocalcinosis
CPPD: pathophysiology
calcium pyrophosphate formed extracellularly
inorganis pyrophosphate reacts with calcium
-> deposits in cartilage (fibrocartilage and hyaline cartilage)
-> inflammation
-> chondrocalcinosis
CPPD: risk factors
age >40 OA Hypothyrodism Hyperparathyrodism Trauma/injury Diuretics Acromegaly Hypomangesaemia Wilson's disease Haemochromatosis
CPPD: clinical features
asymptomatic, accidental finding on X-ray
Red flag: acute tender, red, hot, swollen joint -> acute CPPD (pseudogout)
severe pain and swelling takes 6-24 wks to reach maximum
CPPD: investgations
bloods: WCC, ESR, CRP increased in acute attacks
X-ray: chondocalcinosis, OA changes (LOSS)
USS: CPP deposiion
Aspirate -> positive birefingement rhomboid- shaped crystals under polarized light microscopy
CPPD management
treat underlying cause rest, ice packs -> gradual mobilisation NSAIDs colchicine CS injections
Gout and CPPD comparison: aspirate and joints affected
aspirate: Gout- negatively birefringent cristals, CPPD- positively
joints affected: Gout: usually small joins, CPPD: lage joints
Vasculitis: define
group of heterogenus diseases
inflammation of blood vessels
-> compromise of the vascular lumen
-> ischaemia
Vasculitis: pathophysiology
usually primary -> idiopathic autoimmune disorders secondary - infection (hep B&C, TB, syphilis) - connective tissue disease (e.g. SLE) - drugs (sulphonamides, beta-lactams, quinolones, hydralazine, propylthiouracil)
